Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 112, Issue 11, Pages 3469-3474Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1421975112
Keywords
3q amplification; FXR1; RNA binding protein; non-small cell lung cancer
Categories
Funding
- National Cancer Institute [RO1 CA102353]
- Department of Defense [CDMRP LC090615P3]
- Vanderbilt SPORE in lung cancer [CA 090949]
- Vanderbilt Clinical and Translational Science Award from the National Center for Advancing Translational Sciences [UL1TR000445]
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Aberrant expression of RNA-binding proteins has profound implications for cellular physiology and the pathogenesis of human diseases such as cancer. We previously identified the Fragile X-Related 1 gene (FXR1) as one amplified candidate driver gene at 3q26-29 in lung squamous cell carcinoma (SCC). FXR1 is an autosomal paralog of Fragile X mental retardation 1 and has not been directly linked to human cancers. Here we demonstrate that FXR1 is a key regulator of tumor progression and its overexpression is critical for nonsmall cell lung cancer (NSCLC) cell growth in vitro and in vivo. We identified the mechanisms by which FXR1 executes its regulatory function by forming a novel complex with two other oncogenes, protein kinase C, iota and epithelial cell transforming 2, located in the same amplicon via distinct binding mechanisms. FXR1 expression is a candidate biomarker predictive of poor survival in multiple solid tumors including NSCLCs. Because FXR1 is overexpressed and associated with poor clinical outcomes in multiple cancers, these results have implications for other solid malignancies.
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